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CifA and CifB are Wolbachia-encoded proteins responsible for cytoplasmic incompatibility in Aedes aegypti mosquitoes. CifB (acting as toxin) modifies sperm chromatin in infected males, leading to embryonic death after fertilization of uninfected eggs. CifA (the antidote) rescues embryos when expressed maternally, neutralizing CifB toxicity. These proteins are used in vector control strategies to suppress mosquito populations and reduce transmission of pathogens such as dengue and Zika viruses. The CI mechanism involves aberrant histone-to-protamine exchange during spermiogenesis and subsequent chromatin defects in embryos lacking CifA-mediated rescue[3][4][5][6][7].
CifB modifies paternal chromatin (histone-to-protamine transition) in sperm, resulting in sterility unless maternal CifA is present[3][4][5][6]. CifA binds CifB (in the embryo or egg) and rescues viability by neutralizing CifB toxicity[6][1][4].
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